Evidence map›Paper›PMID 29137254›Full record

ArticleOncotarget2017

Quaking-5 suppresses aggressiveness of lung cancer cells through inhibiting β-catenin signaling pathway.

Xuexia Zhou, Xuebing Li, Cuiyun Sun, Cuijuan Shi, Dan Hua, Lin Yu, Yanjun Wen, Feng Hua, Qian Wang, Qinghua Zhou and 1 more

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed.

  1. Review
  2. RNA-Binding Proteins: Modulators of Canonical Wnt Signaling Pathway.International journal of molecular sciences · 2025
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  17. miR-196b-5p-mediated downregulation of TSPAN12 and GATA6 promotes tumor progression in non-small cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Xuexia ZhouDepartment of Neuropathology, Tianjin Key Laboratory of Injuries, Variations and Regeneration of The Nervous System, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System of Education Ministry, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Xuebing LiTianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Cuiyun SunDepartment of Neuropathology, Tianjin Key Laboratory of Injuries, Variations and Regeneration of The Nervous System, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System of Education Ministry, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Cuijuan ShiDepartment of Neuropathology, Tianjin Key Laboratory of Injuries, Variations and Regeneration of The Nervous System, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System of Education Ministry, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Dan HuaDepartment of Neuropathology, Tianjin Key Laboratory of Injuries, Variations and Regeneration of The Nervous System, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System of Education Ministry, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Lin YuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences of Tianjin Medical University, Tianjin 300070, China.
Yanjun WenDepartment of Neuropathology, Tianjin Key Laboratory of Injuries, Variations and Regeneration of The Nervous System, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System of Education Ministry, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Feng HuaDepartment of Surgery, Shandong Cancer Hospital and Institute, Jinan 250117, China.
Qian WangDepartment of Neuropathology, Tianjin Key Laboratory of Injuries, Variations and Regeneration of The Nervous System, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System of Education Ministry, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Qinghua ZhouTianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
Shizhu YuDepartment of Neuropathology, Tianjin Key Laboratory of Injuries, Variations and Regeneration of The Nervous System, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System of Education Ministry, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Quaking-5 (QKI-5) belongs to the STAR (signal transduction and activation of RNA) family of RNA binding proteins and functions as a tumor suppressor in several human malignancies. In this study, we attempt to elucidate the role of QKI-5 in the pro-metastasis processes of lung cancer (LC) cells and the underlying mechanisms. We confirmed that QKI-5 was decreased in human LC tissues and cell lines, especially in high-metastatic cells. Moreover, QKI expression was positively correlated with LC patients' survival. Functional studies verified that QKI-5 suppressed migration, invasion and TGF-β1-induced epithelial-mesenchymal transition (EMT) of LC cells. Mechanistically, we affirmed that QKI-5 reduced β-catenin level in LC cells via suppressing its translation and promoting its degradation, whereas QKI-5 promoter hypermethylation suppressed QKI-5 expression. Our findings indicate that QKI-5 inhibits pro-metastasis processes of LC cells through interdicting β-catenin signaling pathway, and that QKI-5 promoter hypermethylation is a crucial epigenetic regulation reducing QKI-5 expression in LC cells, and reveal that QKI-5 is a potential prognostic biomarker for LC patients.

Indexed as

lung cancermethylationpro-metastasis processesQKI-5β-catenin

Identifiers

PMID29137254
PMCPMC5669880

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.